Sport accident, trauma and irregular compression of cartilage can result in the damage of articular cartilage, are thought to lead to a loss of cartilage tissue, and without treatment, the injury can progress to OA (Hoemann, 2004). However, articular cartilage has poor repair capacity due to lack of blood supply and limited chondrocyte proliferation. The entrapment of chondrocyte in the dense ECM is thought to reduce chondrocyte proliferation (Huber et al., 2000).
Cartilage injuries are grouped into three main types. The first type is the matrix disruption, caused by blunt force trauma to the tissue which results to damage to the ECM (Zhang et al., 2009). The presence of viable chondrocytes after the damage usually facilitates the recovery of this type of
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injury. Their ECM turnover compensates for the change in durability of the cartilage which effectively increases their synthetic activity to recover the damaged ECM (Temenoff and Mikos, 2000). The second type is the partial thickness defect which only affects the articular cartilage zones and does not permeate to subchondral bone. This defect frequently fails to repair as it does not allow the release of stem cells. Although chondrocytes are present in the cartilage tissue, they fail to move into the defect and proliferate to regenerate the injured region because they are embedded within the ECM (Fuller and Ghadially, 1972; Laurencin et al., 1999). The third type of cartilage injury is the full thickness defect which penetrates through all zones of articular cartilage down to the subchondral bone. This defect allows the release of stem cells such as mesenchymal stem cells (MSC) ‘undifferentiated cells able to differentiate into different cell types’ from the bone marrow into the damaged region and formation of fibrocartilage. Fibrocartilage has mechanical properties that are not the same as articular cartilage (Caplan et al., 1999; Hunziker et al., 1999). It has indeed become necessary to intervene in the repair process due to the low capacity of self- healing or regeneration in damaged articular cartilage. Several surgical methods such as debridement, microfracture, autografts and cell therapy approaches like autologous chondrocyte implantation (ACI) have been employed to provide pain relief and improve joint function (Schurman et al., 2000).
Debridement
Debridement involves removing the roughness of the cartilage surface by cleaning and smoothing the defect area in the knee joint. While this technique is easy to perform, the result is still questionable as only temporary improvements are usually experienced among patients with advanced stages of degeneration (Jackson et al., 2003).
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Microfracture
Microfracture is a commonly employed method for repairing articular cartilage of patients having lesions less than 2 cm in diameter (Zhang et al., 2009). It is a less invasive process with short surgery and recovery time compared to other treatments (Clair et al., 2009). Microfracture involves boring a hole through articular cartilage and the subchondral bone to release bone marrow stem cells to the damaged site (Redman et al., 2005). Instead of the fibrin clot, the MSC which are gradually fill the lesion site and then totally fill the injured site after one week (Hunziker et al., 1999). Over time, most of these MSCs can differentiate to chondrocytes, which then secrete articular cartilage proteins into ECM and repair the damaged articular cartilage site (Redman et al., 2005). The main disadvantage of this method is the production of fibrocartilage with weaker mechanical properties that are not suitable for articular cartilage, which is linked with increased failure rate (Laurencin et al., 1999; Zhang et al., 2009).
Autograft transplantation
In this technique, a full depth plug of tissue is collected from non-weight bearing area in the joint of the patient, followed by an implantation process into damage region of joint in order to obtain healthy tissue graft (Clair et al., 2009). In spite of the excellent medical outcomes using this autografting method, there are some shortcomings which include inadequate donor tissues both in terms of capacity and quality, donor area morbidity (Laurencin et al., 1999). Also, stability of the graft tissue at high weight-bearing region over time as a result of the graft tissue being extracted from a non-weight bearing area (Malloy et al., 2002).
Total and partial joint replacement
When other methods fail to repair the cartilage damage or when the articular cartilage has severe damage and advanced joint disease, then either total or partial joint replacement are employed. This
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method is done to restore typical function by removing the injured joint and implanting artificial shell (such as alloys and titanium), a polymer surface (such as polyethylene) as well as a metal stem. However, it comes with its own limitations including loosening of the artificial implant, wearing off and short life-span of implant (maximum of 15 years) and increasing pain of the patient (Zhang et al., 2009).
Autologous chondrocyte implantation
Autologous Chondrocyte Implantation (ACI) is a process in which cells are harvested from the donor site within the injured joint, expanded in vitro and re-injected into the defect site under a natural or synthetic patch (Brittberg et al., 1994). ACI has evolved over the last 20 years and as result of its 80% clinical success rate (Mistry et al., 2017). This method is the first cartilage tissue engineering approach to be applied clinically, and cartilage tissue engineering is presently aimed at improving the method and outcomes using different cells, materials, and culture environments (Brittberg et al., 1994).
Brittberg et al (1994) were the pioneers of the Autologous Chondrocyte Implantation (ACI) for cartilage. The ACI technique has been applied by different generations for several years (Marlovits et al., 2006). The first generation of ACI is the Brittberg’s technique which is based on two surgical processes. The first process involves the removal of a small piece of undamaged articular cartilage tissue, isolation of chondrocytes and their expansion in vitro to the required number of cells. In the second process, the cells are injected into the damaged region of articular cartilage and sutured by periosteal patch as a cover to ensure chondrocytes are within the defected area (Brittberg et al., 1994). In the second generation of ACI, the cells are placed on a collagen matrix instead of the periosteal patch after being expanded in a monolayer. A collagen matrix is sutured over the cartilage lesion and the cell suspension is injected beneath (Haddo et al., 2004). In the third generation of ACI, the chondrocytes are spread homogeneously into the defect by placing their
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suspension on a 3D biomaterial scaffold, and grafting is done using fibrin glue (Marlovits et al., 2006). The whole surgical morbidity is minimized in the second and third generation of ACI as they facilitate the surgical process as well as reduce the surgical time and number of injury cases (Marlovits et al., 2006). In spite of the favourable outcomes recorded, this technique has a number of limitations such as the possibility of producing fibrocartilage, which has a different mechanical property from hyaline cartilage and requires multiple invasive surgeries. Also, it reduces the long term stability (Zhang et al., 2009).